Our studies have generally been focused on the nature of defensive and regenerative mechanisms which can be activated in response to ischemic injury, as well as on potential therapeutic manipulation of such defensive responses. In these studies we were able to demonstrate participation of brain-derived neurotrophic factor (BDNF) in the development of enhanced neuronal resistance to ischemic injury, demonstrable 3 days after induction of the spreading depression in the cortex. In therapeutic trials, BDNF was administered via the microcanullae inserted sterotaxically into the ventral thalamic region of the rat subjected to cardiac arrest cerebral ischemia (CACI). The delivery of the BDNF commenced 3 days before the CACI and lasted till the sacrifice of the animal at 7 days after cardiac arrest. Using specific monoclonal antibody for GABA demonstrated a striking proliferation and sprouting of GABAergic terminals in the ventral thalamic nucleus in the vicinity of the site of BDNF delivery. Also, there was a conspicuous preservation of GABAergic neurons of the nucleus reticularis thalami on the side of BDNF application.